Windy City Medic responded to Cardiac Arrest Management is an EMT-Basic Skill – The BLS Evidence with –
I think the cartoon you posted is an excellent way of illustrating your stance, and the entire premise of evidence-based medicine, not only on this issue, but on many others as well.
Thank you, but it is something that many people do not seem to understand.
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The point is that a treatment being performed without any evidence supporting the efficacy of said treatment is not treatment at all, but voodoo medicine.
Voodoo medicine is not medicine.
Medicine is much more than wishful thinking.
We assume that we wouldn’t be using a treatment unless we know it works.
If we know it works, it is because we can provide good evidence.
If we can’t provide good evidence, then it is voodoo.
If the evidence provided does not show improved survival, then we must demand evidence of improved survival or we must put a time limit on the use of the treatment.
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This applies to the use of selective cardiotoxins in the case of dysrhythmias, high-flow O2, spinal immobilization, the three nitro rule, Lasix for CHF or hypertensive crisis, etc. Many people are still of the opinion that we should do everything that we think MIGHT work on the off chance that something WILL work, and don’t stop to consider that some of those “treatments” may actually lead to worse outcomes than withholding that treatment in the first place.
Selective cardiotoxins (such as lidocaine) and non-selective cardiotoxins may cause worse rhythms. The more we learn about antiarrhythmics, the more selective we are about which patients should be exposed to this risk.
Supplemental oxygen may cause damage. The more we learn about oxygen, the more selective we are about which patients should be exposed to this risk.
Long spine board immobilization causes damage. The more we learn about long spine board immobilization, the more selective we are about which patients should be exposed to this risk.
The 3 nitro rule harms patients. The more we learn about the uses of nitroglycerin, the more aggressive we become in treating patients with this life-saving treatment.
Lasix (furosemide) is not an drug that should be used to treat unstable CHF/ADHF (Congestive Heart Failure/Acute Decompensated Heart Failure). The more we learn about Lasix, the less likely we are to give this drug to unstable CHF/ADHF patients.
All things are poison and nothing is without poison, only the dose permits something not to be poisonous. – Paracelsus.
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For example, there is a school of thought that therapeutic hypothermia works in part because it slows the damage caused by high doses of epinepherine. That 80mg of Lasix might put someone on dialysis for the rest of their life, if it doesn’t send them into outright renal failure. Withholding NTG may just kill someone.
That may be the case.
The problems with epinephrine are not that simple. We are taught to automatically give it to every patient who does not have a pulse after the first defibrillation and to every PEA/asystole patient.
This is not medicine. There is no assessment of whether epinephrine might be in the patient’s best interest. There is no consideration that the adult patient has an SVT at 280 QRS complexes per minute, but we are not able to palpate pulses, and a drug to speed up the heart might not be a good idea. According to the PEA algorithm, the treatment is epinephrine, more epinephrine, and a lot more epinephrine – unless the patient has ROSC (Return Of Spontaneous Circulation).
But we are not supposed to allow our assessment to interfere with this catecholamine marinade. If we can identify a specific H or T to treat, we just add the H or T antidote to the mix.
Cardiac arrest due to cocaine overdose? Then give one of the closest things we have to cocaine – massive doses of epinephrine.
Cardiac arrest due to a heart attack (this means about half of the cardiac arrests we treat)? Then give one of the most dangerous drugs we have for heart attack – massive doses of epinephrine.
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The point of the matter MUST be that continuous, uninterrupted chest compressions and timely defibrillation (provided that defibrillation doesn’t interfere with the delivery of chest compressions) are the ONLY treatments shown to improve survival to neurologically-intact hospital discharge.
So far.
The other treatments we use may provide benefit, but we refuse to find out.
There have been very few studies trying to figure out if ALS treatments work.
No study of any ALS treatment
has shown significant improved survival
to discharge with a functioning brain.
Ever.
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Therefore, any other treatments dictated by local protocol should be timed in such a way as to minimize interruption of chest compressions and prevent delayed defibrillation.
One problem is that the local protocol, which should not include these treatments, generally wants these treatments given as quickly as possible.
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Local protocols will indeed continue to dictate our treatment pathways, but we as paramedics need to remain educated and take steps in our own treatment pathways to integrate what has been proven to WORK with what our protocols require.
The more we educate those who determine the way the ACLS guidelines are written. Almost everyone automatically follows the ACLS pied piper.
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That means doing continuous chest compressions until we have enough personnel present to do all of the “paramedic stuff” while someone else does the chest compressions. Minimize interruptions. Start the line and push the drugs while someone maintains continuous chest compressions. Intubation should be performed with compressions ongoing, and if that’s not possible, then it should be done during a rhythm check, not during an otherwise-unnecessary interruption in CPR. Go for IO access if you can’t get a line, consider a King Tube or other blind-insertion airway device if your protocols dictate that you use an advanced airway. CONTINUE CPR while the defibrillator is charging and resume it IMMEDIATELY after administering the shock.
Or just do excellent compressions and delay those harmful treatments as long as possible and almost all of the patients with a good chance at surviving past discharge should already be resuscitated.
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A lot of people seem to have difficulty separating ACLS guidelines from local protocols and have an even harder time integrating what has been proven to WORK with what their guidelines and protocols tell them they have to do. No one is advocating that Paramedics should go rogue (Ha!) and start doing things their own way. I think Rogue is advocating for systemic change in the way we treat cardiac arrest, and we as medical professionals have the responsibility to try to integrate our protocols and guidelines with what we know will work. Maybe then, we’ll hit on something huge.
We should be demanding that our medical directors allow us to provide treatments that work, rather than just providing wishful thinking left over from the Dark Ages of EMS.
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Those medical directors that refuse to allow us to think, and keep us in those Dark Ages of EMS should politely be shown the door.
“Rampart, can I get some Bicarb?”
CCC,
Amen.
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Medical command permission is an example of poor judgment from medical directors.
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I have been working on a post of my own on this topic. Meanwhile, thank you for your reply.
Now posted at windycitymedic.blogspot.com
Thanks again, I am thoroughly enjoying this discussion.
I am again as a non professional speaking out about how sudden cardiac arrest victims are handled. First of all, I don’t envy first responder’s having to know more than one set of standards. The responsiblity of initial evaluation is overwhelming and until we have star trek like medical instruments, you will have to make educated guesses at what is up.
My sudden Cardiac Arrest was not CAD related rather due to Broken heart syndrome. The EMS team said they had never seen such weird EKG and the AED was confused also. So,do you follow your perscribed protocol in a situation that doesn’t fit any model? So what pathway do you follow? what meds do you use?
I have such strong feelings about continued compressions due to thier success rate that all of the other protocol seems too cumbersome. I guess that since I’m not most people, maybe someone communicating from the er was interpreting the info. Regardless, according to my cardiologist, the continued compressions saved my life.
I feel your pain and wonder if there can be a basic standard and in the stiuation of good communication with the receiving facility, decisions about additional treatments can be rationally be made.
Ultrasound could help differentiate Tako-Tsubo cardiomyopathy from a more traditional CAD related insult to the heart, however, in the case of a sudden cardiac arrest this isn’t going to be possible. The honest answer is you work what we call the H’s and T’s. Basically, we take the history and we attempt to direct our efforts towards reversing reversible causes.
So, is there really any difference in the prehospital care of SCA from HCM versus CAD? The answer is no.
1. Continuous, uninterrupted CPR
2. Defibrillate VF/VT
3. Repeat until ROSC
Bravo ! Loved reading this post and highly agree. There is too much knowledge and technology available not to use them for the benefit of our patients and our profession.
Let me begin by saying that I absolutely agree with the underlying premise that any intervention we perform should absolutely be supported by high quality, well designed studies. The lack if such research for many/most ALS interventions is arguably voodoo medicine. That being said, in the presence of cardiac arrest without a research supported intervention (I.e. a systole and PEA outside obvious reversible causes), is it possible to design an ethical study to determine the effectiveness of vasopressors? I would concede that VF/VT could be studied with simply CPR and Defibrillation, but with a systole and especially PEA, would withholding vasopressors be unethical as there is no logical reason to do so?